瘦素缺乏小鼠椎间盘退变的组织学观察  

Histologic observation of intervertebral disc degeneration in lack-leptin mice

作　　者：郭震[1] 李新锋[1] 戴力扬[1] 

机构地区：[1]上海交通大学医学院附属新华医院骨科,上海200092

出　　处：《脊柱外科杂志》2012年第2期113-117,共5页Journal of Spinal Surgery

摘　　要：目的探讨瘦素在椎间盘退变中的可能作用。方法采用HE染色观察6月龄雄性ob/ob小鼠(瘦素缺乏小鼠)和野生型小鼠(C57BL小鼠)椎间盘的形态学;免疫组织化学检测Ⅱ型胶原、蛋白聚糖的表达;Real-time PCR检测Ⅱ型胶原、Ⅹ型胶原及蛋白聚糖的基因表达。结果与野生型小鼠相比,ob/ob小鼠椎间盘HE染色表现为椎间盘组织的胶原结构紊乱、髓核碎裂、椎间盘高度降低,免疫组化检测显示Ⅱ型胶原、蛋白聚糖表达减少,Real-time PCR检测显示Ⅱ型胶原、蛋白聚糖基因表达下调而Ⅹ型胶原基因表达上调,差异有统计学意义(P<0.05)。结论活体内瘦素缺乏可能加速小鼠椎间盘退变。Objective To explore the possible role of leptin in intervertebral disc degeneration.Methods The intervertebral discs of 6-month-old male ob/ob mice(lack-leptin mice) and wild type mice(C57BL mice) were histologically observed by HE staining.The expression of collagen Ⅱ and aggrecan were detected by immunohistochemistry.And the gene expression of collagen Ⅱ,collagen Ⅹ and aggrecan were measured by Real-time PCR.Results HE staining results showed collagen disorders,fragmentation of nucleus pulposus,and decreased height of intervertebral disc in ob/ob mice.Compare with the wild type mice,there were decreased protein level of collagen Ⅱ and aggrecan,downregulated mRNA expression of collagen Ⅱ and aggrecan,and upregulated mRNA expression of collagen Ⅹ in ob/ob mice.There was significant difference of the changes between wild type mice and ob/ob mice(P<0.05).Conclusion In vivo,lack of leptin may accelerate intervertebral disc degeneration in mice.

关 键 词：椎间盘 免疫组织化学 瘦素 小鼠 

分 类 号：R681.53[医药卫生—骨科学]